Translation of the abstract (English)

Crosstalk between melanocytes and keratinocytes is important in the human epidermis. It is known that the normal melanocytic phenotype and controlled proliferation of melanocytes is strictly regulated by keratinocytes via E-cadherin. Malignant transformation of melanocytes frequently coincides with loss of E-cadherin expression and the upregulation of N-cadherin.
This leads to the loss of ...

Translation of the abstract (English)

Crosstalk between melanocytes and keratinocytes is important in the human epidermis. It is known that the normal melanocytic phenotype and controlled proliferation of melanocytes is strictly regulated by keratinocytes via E-cadherin. Malignant transformation of melanocytes frequently coincides with loss of E-cadherin expression and the upregulation of N-cadherin.This leads to the loss of regulatory dominance by keratinocytes. Further, melanoma cells can now get into contact with fibroblasts via N-cadherin and induce e.g. MMP expression.Previously, we could show that N-cadherin, which is strongly expressed in melanoma cells leads to a consistiently NFkappaB expression and after transiently transfection of full length E-cadherin the NFkappaB activity is strongly reduced. Furthermore, transient transfection of cytoplasmic beta-catenin into the melanoma cells leads to upregulated NFkappaB activity. The cytoplasmic beta-catenin in melanoma cells leads to upregulation of p38 MAP-kinase activity and this leads to transcriptional activity of NFkappaB. The target gene of NFkappaB is N-cadherin.